Topic 10: Avian diseases caused by circovirus, Chicken infectious anemia Flashcards
Avian Circoviruses
Circoviridae, Genus circovirus
- PBFDV, PiCV, GoCV
Genus gyrovirus
- CAV, chicken infectious anemia
PBFDV - Epidemiology
Australia, 1984, most prevalent in austarralian species, eg cockatoos
Young psittacine birds (old and new world parts) under 3 years susceptible
Horizontal and vertical transmission
vertical acquired from nestlings of the parents fo germinative
horizontal from other flock members
Virus can be found, spread through crop secretions (crop milk), faeces and feather follicles and skin particles
Adult birds develop resistance when infected, but will be life long shedders
sound birds more susceptible, weaker immune system
Pathogenesis PBFDV
infection, viraemia, reaches all organs
attacks feather follicles and dividing cells of beak and claws, progressive beak feather and claw malformation nd necrosis
later, feather shaft constriction hampers feather development until al death growth stops
also causes degeneration of lymphoid tissues, thymus and bursa fabricci , immunosuppression, 2º infection
locus minors resistência, beak and claw lesions
also affects the gut epithelial cells, vom , dra
CS of PBFDV
Young psittacines, under 3 yrs susceptible
- specifically at 2-10w
acute form
- lethargy anorexia, vom, dra, nasal discharge
- depression, inappetence
- severe immunosuppression , multiple 2ºinfections, dead within 2-4 weeks, typically before lesions on beak and
- 10-70% losses
Chronic
- may last for years
- if the bird manages to mount an immune sresponse
characteirics changes after 1st moult, require time to develop
- loss of feathers, broken beak, soft beak, no feather son neck or back
Surviing birds are lifelong shedders
Dx of PBFDV
CS, PM Lesions and HP
avian circoviruses cannot be cultured!
PCR, nucleotide sequence
Cross infections with other genotypes of other birds, goose, duck pidgeon etc
different pathogenicity
Tx of PBFDV
no Tx, only treat 2º infection,
Euthanisa recommended
Prevention of PBFDV
hygiene prevention 2º infection with ab Vx with inactivated virus quartile new birds and test known carrier should not be introduced to new pens
PiCV Epidemiology
NA, 1993, now WW
Young pigeon, mostly under 1 year ( esp. up to 4m)
–> Young pigeon disease syndrome, YPDS
Germinative
Horizontal, spread through the droppings or by inhalation
PiCV Pathogenesis
Targets lymphoid organs, thymus, spleen, bone marrow, bursa fab. –> Immunosuppression, failure to overcome 2º , common or harmless infection
CS / Symptoms PiCV
Generalised no specific lesions, similar BFD, lethargy, anorexia, WL, dra, resp
Death within 2-5 days (can be 100% mortality in young pigeons
Retarded growth
Rarely beak, claw and feather deformities
Poor performance (racing)
symptoms depend on the severity of the 2º infection, age of infection
Infection can be asymptomatic
Dx of PiCV
PCR of internal organs (PM), faeces
Tx of PiCV
no Tx, only of 2º infection
Prevention
Prevent contact with virus, hygiene, quarrantine etc
GoCV, Goose Circovirus
GoCV, affects geese under 1w, growth retardation, decreased production, feathering problems, increased mortality due to 2º infections
Co infections with Riemerella anatipestifier and aspergillum fumigates can occur
CAV Aetiology
Japan, 1979, now WW esp countries where chickens are raised commercially
causes anemia and immunosuppression
Single serotype, only chickens affected
Circoviridae, Gyrovirus
- genome codes for 3 VP , viral proteins
- VP1, capsid proteins
- VP1 and 2, protein phosphatase
- VP3, induces apoptosis in infected cells
resistance, 80º up to 30 mins
CAV Epidemiology
Horizontal, faeco oral, respiratory via infected feather follicle epithelium
Vertical, via egg, semen of roosters
vx of seronegative flocks before onset of egg production is recommenced to prevent vertical transmission
Virus is shed via the egg and faeces for up to 2 months (max shedding week 2 PI)
maternal ab negative chicks are susceptible to disease until 3w
postive are protected
under 3 weeks, disease, sever imuunosuprrseion
over 3w, no disease, mild immunosuprrseion
CAV Pathogenesis
PO, Intestine, fireman, within 24hrs, to organs and tissues
Bone marrow, erythroid and myeloid cells, anemia, immunosupression
thymus, Bursa fabricius, immunosupression
Platelets, haemorrhages, lymphoid cell necrosis
other organs
Immunosuprrseions leave the bird liable to 2º infection
- E.coli, mycoplasma, adenoviruses, reoviruses
CS CAV
Clincialy affected birds, anemia dermatitis syndrome in 10-14 day old chicks, rare,following vertical or horizontal transmission
Sub clinical: after horizontal, resistance develops with age, decreased productivity
Most susceptible are MAtab negative, 1-4 w
incubation of 7-10d
clinical disease only apparent in ab negative chicks up to 1m
Atypical signs, anorexic chicks, lethargic, inappetence, depressed and pale with anema, low icv, blood may be watery and clot slowly
retarded growth
Variable mortality, 10-50% , higher with 2º infection
Pathology of CAV
pale tissues, haemorrhages thought the body
anemia, oedema, haemorrhages, under skin, gizzard, proventriculs
atrophy of the bursa and thymus 10-14 days after vertical transmission
pale and yellow bone marrow
necrotic regions in the liver
HP of CAV
myeloid and lymphoid cell depletion
Dx of CAV
Cs, pathology, gross lesions, only suspicion of disease, need further diagnostic testing
culture in chicken lymphoblast cell line and chicken embryos
virus isolation in lymphoid cell cultures
IF, PCR, VN, ELISA, IP
Ddx of CAV
Infectious bursa disease, (dra, more intense bleeding, thymus only mildly affected)
Newcastle DV
inclusion body hepatitis, necrosis, bleeding, pancreas liver and spleen
Tx of CAV
no treatment, only 2º bacterial infection
Prevention and control
general preventative ruiles, hygiene
Vx via drinking water at 12-15 days
- live (moderately attenuated vx) fo Ab negative breeder flocks @ 12-15 w , prior to egg production
IM/SC vx over 2w, but min 6 weeks before laying
